Hexeberg S, Hexeberg E, Willumsen N, Berge R K
Department of Anatomy and Cell Biology, University of Bergen, Norway.
Br J Nutr. 1994 Feb;71(2):181-92. doi: 10.1079/bjn19940125.
Pectin is known as a cholesterol-reducing dietary fibre, and in the present study we addressed the question whether pectin affected the quantity of lipid in droplets in the myocardial cells and of lipid in the liver cells. Male Wistar rats received either a diet containing cholesterol or a standard diet without cholesterol with 0, 50 or 100 g pectin/kg incorporated for 10 d. The fractional volume of lipid droplets in the myocardial cells decreased as a function of pectin dose in both the standard-fed and the cholesterol-fed rats. Serum cholesterol was significantly reduced in both groups after addition of 100 g pectin/kg diet. The cholesterol diet increased the liver cholesterol level, and 100 g pectin/kg diet resulted in a lower concentration of liver cholesterol in the cholesterol-fed animals, but the influence on standard-fed rats was modest. Hydroxymethylglutaryl-CoA reductase (EC 1.1.1.88; HMG-CoA reductase) activity increased when pectin was given in the standard diet. Liver triacylglycerol level increased after cholesterol and pectin feeding. Mitochondrial fatty acid oxidation and phosphatidate phosphohydrolase (EC 3.1.3.4) activity tended to decrease, whereas the peroxisomal fatty acid oxidation and acyl-CoA oxidase activity were unchanged. Increased hepatic triacylglycerol content by cholesterol and pectin treatment may be due to inhibited mitochondrial fatty acid oxidation along with increased availability of fatty acid for esterification and triacylglycerol synthesis. The presence of pectin in the diets of cholesterol-fed rats resulted in increased hepatic concentration of triacylglycerols and increased mitochondrial fatty acid oxidation. In this case the hepatic accumulation of triacylglycerol may be mediated by a reduced efflux of triacylglycerols from the liver.
果胶被认为是一种可降低胆固醇的膳食纤维,在本研究中,我们探讨了果胶是否会影响心肌细胞和肝细胞中脂滴内的脂质含量。雄性Wistar大鼠分别接受含胆固醇的饮食或不含胆固醇的标准饮食,标准饮食中添加0、50或100 g/kg果胶,持续10天。在标准饮食组和胆固醇饮食组中,心肌细胞中脂滴的分数体积均随果胶剂量的增加而降低。在饮食中添加100 g/kg果胶后,两组大鼠的血清胆固醇均显著降低。胆固醇饮食会提高肝脏胆固醇水平,在胆固醇饮食组中,100 g/kg果胶饮食可使肝脏胆固醇浓度降低,但对标准饮食组大鼠的影响较小。在标准饮食中添加果胶时,羟甲基戊二酰辅酶A还原酶(EC 1.1.1.88;HMG-CoA还原酶)活性增加。胆固醇和果胶喂养后,肝脏三酰甘油水平升高。线粒体脂肪酸氧化和磷脂酸磷酸水解酶(EC 3.1.3.4)活性有降低趋势,而过氧化物酶体脂肪酸氧化和酰基辅酶A氧化酶活性未改变。胆固醇和果胶处理导致肝脏三酰甘油含量增加,可能是由于线粒体脂肪酸氧化受到抑制,同时用于酯化和三酰甘油合成的脂肪酸可用性增加。在胆固醇饮食组大鼠的饮食中添加果胶会导致肝脏三酰甘油浓度升高,线粒体脂肪酸氧化增加。在这种情况下,肝脏三酰甘油的积累可能是由肝脏中三酰甘油流出减少介导的。